期刊文献+

硫酸多糖916对细胞因子和H_2O_2 诱导ECV304细胞产生一氧化氮的影响(英文)

Effect of polysaccharide sulfate 916 on the production of nitric oxide in ECV3 04 cells induced by cytokines and H_2O_2
原文传递
导出
摘要 目的 研究硫酸多糖 916 (PS916 )对TNFa、IL 1β和H2 O2 诱导ECV30 4细胞产生一氧化氮 (NO)的影响。方法 用Griess试剂测定ECV30 4细胞产生的NO ,用MTT法测定细胞的增殖 ,用荧光法测定NO合酶的活性。结果  4 0ng/mlTNFa和 4 0ng/mlIL 1β使ECV30 4细胞NO产生下降 ,0 1mmol/LH2 O2 使NO的产生增加。PS916剂量依赖性增加TNFa、IL 1β诱导的ECV30 4细胞NO的产生 ,降低H2 O2 诱导ECV30 4细胞产生的NO。TNFa和H2 O2 抑制ECV30 4细胞的增殖 ,而IL 1β对ECV30 4细胞的增殖没有明显影响。PS916剂量依赖性的抑制TNFa和H2 O2 的作用 ,增加存活细胞数。在体外 ,PS916对细胞的NO合酶无明显的影响。结论 PS916在体外实验中对细胞因子和H2 O2 引起的ECV30 4细胞损伤有拮抗作用 ,对细胞表现出明显的保护作用。 To investigate the effect of polysaccharide sulfate 916 (PS916) on the productio n of nitric oxide (NO) in ECV304 cells induced by tumor necrosis factor α (TNF α), interleukin 1β (IL 1β) and H 2O 2 in vitro Methods Production of NO in ECV304 cells was measured by the Griess method and the proli feration of cells was tested by the MTT method The activity of NO synthase was detected spectrophotometrically Results Production of NO in ECV304 cells decreased after treatment with 40?ng/ml IL 1 β and 40?ng/ml TNFα, but increased in the presence of H 2O 2 0 1?mmol/L PS916 significantly enhanced NO production in ECV304 cells in a dose depende nt manner in the TNFα and IL 1β treated groups and decreased it in the H 2O 2 treated group Proliferation of ECV304 cells was inhibited by TNFα and H 2O 2 and no effect was found in the IL 1β treated group PS916 increased the proliferation of cells treated with TNFα and H 2O 2 dose dependently In vitro, PS916 has no effect on the activity of NO synthase Conclusion PS916 has a protective effect on ECV304 cells exposed to IL 1β, TNFα and H 2 O 2
出处 《Chinese Medical Journal》 SCIE CAS CSCD 2002年第4期614-619,共6页 中华医学杂志(英文版)
基金 theNationalNaturalScienceFoundationofChina (No 3 0 0 1161940 )
关键词 ECV304 硫酸多糖916 一氧化氮 H2O2 ECV304 cells . polysaccharide sulfat e 916 . nitric oxide . cytokines
  • 相关文献

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部